Thromb Haemost 1973; 30(01): 025-035
DOI: 10.1055/s-0038-1649099
Original Article
Schattauer GmbH

Induction of Disseminated Intravascular Coagulation in the Factor XII-deficient Fowl

Morphological Effects of Liquoid, Bacterial Endotoxin and Tissue Thromboplastin in the Normal and Anticoagulated Fowl
Fredrik Skjørten
1   Ullevål Hospital, Department of Pathology (Head: K. Arnesen M.D.), University of Oslo and Rikshospitalet, Medical Department A, Section of Haematology (Head: P.F. Hjort M.D.), University of Oslo, Oslo, Norway
,
Stein A. Evensen
1   Ullevål Hospital, Department of Pathology (Head: K. Arnesen M.D.), University of Oslo and Rikshospitalet, Medical Department A, Section of Haematology (Head: P.F. Hjort M.D.), University of Oslo, Oslo, Norway
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Publikationsverlauf

Received for publication 30. Januar 1973

Accepted for publication 30. März 1973

Publikationsdatum:
30. Juni 2018 (online)

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Summary

Birds are naturally deficient in the coagulation factors responsible for the contact activation reactions in mammalian plasma. In the present study, fowl lungs were examined for evidence of disseminated intravascular coagulation (DIC) 5 min or 4 hours after injection of either Liquoid or bacterial endotoxin. These substances are potent initiators of DIC in mammals, and activation of factor XII is believed to be essential for their triggering effect.

Liquoid injection produced intravascular deposits with the light microscopical staining properties of fibrin. However these deposits had a purely granular ultra-structure; their formation was not prevented by adequate anticoagulation, and there was no concomitant thrombocyte aggregation. It is suggested that the deposits represent precipitates of plasma proteins, including fibrinogen.

Endotoxin failed to produce clinical reactions, intravascular deposits or thrombocyte aggregates. In contrast, animals injected with homologous tissue thromboplastin died, and fibrillar material with the ultrastructural appearance of fibrin, as well as thrombocyte aggregates were found in small pulmonary vessels. These effects were completely prevented by anticoagulation.

We conclude that both Liquoid and endotoxin failed to trigger DIC in the factor XII-deficient fowl, suggesting that these substances depend on the contact activation reactions for the generation of thrombin.